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Academic literature on the topic 'Interferoni'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Interferoni"

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Cavallo, Giorgio, Marisa Gariglio, Saverio Panico, and Santo Landolfo. "Regolazione delľ espressione genicain vivo da parte degli interferoni." Rendiconti Lincei 1, no. 1 (March 1990): 105–9. http://dx.doi.org/10.1007/bf03001755.

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Betterle, Corrado, and Fabio Presotto. "Terapia con interferoni e autoimmunità organo-specifica: quali rischi e come gestire il paziente." L'Endocrinologo 11, no. 5 (October 2010): 198–206. http://dx.doi.org/10.1007/bf03344741.

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Larsen, Thomas Stauffer, Michael Boe Møller, Karin de Stricker, Peter Nørgaard, Jan Samuelsson, Claus Marcher, Ole Weis Bjerrum, Morten T. Andersen, and Hans Carl Hasselbalch. "Minimal Residual Disease and Normalization of the Bone Marrow after Long-Term Treatment with Alpha-Interferon2b in Polycythemia Vera. A Report on Seven Patients in Sustained Complete Hematological Remission with Major Molecular Responses." Blood 112, no. 11 (November 16, 2008): 1744. http://dx.doi.org/10.1182/blood.v112.11.1744.1744.

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Abstract Background : Polycythemia vera (PV) is a clonal myeloproliferative disorder characterized by the presence of the JAK2V617 mutation in virtually all patients. Recently several studies have shown that the JAK2V617F mutational load decreases during treatment with alpha-interferon2 (1–6). Aim: To report on molecular and histomorphological bone marrow responses in seven PV patients with complete molecular remissions during and after long-term treatment with alpha-interferon 2b. Patients: Seven patients treated with alpha-interferon2b for a median of 84 months (range 31–120) are reported. In four of the patients alpha-interferon2b was started at the time of diagnosis and in three patients 9, 36 and 42 months from the time of diagnosis, respectively. Methods: The mutation was determined by allele specific PCR (n=2 only) (7) and quantitative PCR (qPCR) (n=5) (8). In three out of these patients qPCR JAK2V617F was performed on archived bone marrow from diagnosis (2 patients) and on peripheral blood (one patient) prior to treatment with alpha-interferon2b. A complete molecular remission (CMoR) was defined by less than 2 % JAK2 V617F mutated alleles (7). Results: Molecular Responses. All patients obtained a CMoR after a median of 84 months (29–120 months) of treatment with alpha-interferon2b. Subsequently all patients have discontinued alpha-interferon with a follow-up period of median 10 months (range 4–30 months) and sustained complete hematological remission. Furthermore, in three patients molecular responses have recently been updated – April and May 2008 - showing CMoRs in all (1,2 %, 0,9 % 0,1 % mutated alleles, respectively). Bone Marrow Responses. Follow-up bone marrow biopsies were available in five patients. Complete normalization of the bone marrow was seen in three patients after treatment with alpha-interferon2b for 84, 132 and 132 months, respectively. In the bone marrow from the patient being treated with alpha-interferon for 132 months a qPCR JAK2V617 analysis was performed detecting the mutation at a very low level (0,5 % mutated alleles). In two other patients, being treated with alpha-interferon2b for 24 and 120 months, respectively, and having obtained a CmoR in peripheral blood the bone marrow histomorphology showed marked regression of PV-features but in both patients still with focal areas displaying an increased number of morphologically abnormal megakaryocytes. Updated histomorphological and molecular response patterns will be presented. Discussion and Conclusion : Previous studies on the molecular response during alpha-interferon2a treatment have shown that a substantial proportion of patients achieve a significant molecular response after 12 months with a continuous decrease in the JAK2V617F mutation load at 24 and 36 months (1,5,6). This report confirms and extends preliminary data, showing that long-term treatment with alpha-interferon 2b in a subgroup of PV-patients is able to induce complete molecular remissions with normalization of the bone marrow morphology, which may even be sustained after discontinuation of alpha-interferon2b for up to 20 months (5). Prolonged treatment for several years seems necessary to induce such sustained responses, since treatment for only a few months has been reported to be followed by rapid recurrence of clonal hematopoiesis (9). In conclusion, a state of “minimal residual disease” may be achieved in PV by long-term immune therapy using alpha-interferon 2. Our observations call for large prospective clinical studies in which treatment with alpha-interferon is initiated up-front in patients with JAK2-positive PV and allied diseases. These studies should also aim at exploring the minimal dose of alpha-interferon needed to elicit complete molecular responses in order to minimize side effects of the drug and accordingly diminish the high drop-out rates reported in most previous studies.
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Muttar, A. A. "Cloning and gene expression equine leukocyte α-interferon in cells of Escherichia Coli." Al-Qadisiyah Journal of Veterinary Medicine Sciences 12, no. 1 (June 30, 2013): 82. http://dx.doi.org/10.29079/vol12iss1art234.

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Interferon plays role in innate immune responses through upregulation of costimulatory molecules and induction of proinflammatory cytokines. interferons including interferon alpha (IFNA). The present study characterized IFNA cDNA and predicted protein. The interferon’s play a great role in protection from infections, which have been called by microorganisms, and also have powerful antiproliferation and immunomodulation activity. The purposes of study: cloning and expression of horse leukocyte interferon and purification the product protein. The results and discussion : In the result we isolated (DNA) from equine leukocyte in blood, which was used in the quality of the matrix for amplification of α-interferon gene with PCR HELP, and isolation gene α-interferon and transformation in vector puc18 and expression vector PET24b (+) and recombinant plasmid was transformed into E. coli strain BL21( codon plus 440) induction with IPTG. The results showed the protein having the same molecular weight as horse interferon alpha about 5.81 kDa
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Zimring, James C., Stephen Goodbourn, and Margaret K. Offermann. "Human Herpesvirus 8 Encodes an Interferon Regulatory Factor (IRF) Homolog That Represses IRF-1-Mediated Transcription." Journal of Virology 72, no. 1 (January 1, 1998): 701–7. http://dx.doi.org/10.1128/jvi.72.1.701-707.1998.

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ABSTRACT Human herpesvirus 8 (HHV-8) is the probable viral etiologic agent for Kaposi’s sarcoma. The HHV-8 genome encodes viral interferon regulatory factor (vIRF), a gene product that has homology to the IRF family of transcription factors. We demonstrate that vIRF inhibits responses to type I and type II interferons and blocks IRF-1-mediated transcription. vIRF does not compete with IRF-1 for binding to DNA or complex directly with IRF-1. The ability of vIRF to block IRF-1-mediated transcription is independent of the DNA binding domains of both vIRF and IRF-1. These data suggest that vIRF may contribute to viral pathogenesis and cellular transformation by interfering with interferon- and IRF-1-mediated gene expression through a novel mechanism.
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Foley, John F. "Interfering with interferons." Science Signaling 9, no. 415 (February 16, 2016): ec30-ec30. http://dx.doi.org/10.1126/scisignal.aaf4271.

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Wilks, J., and T. Golovkina. "Interfering with interferons." Science 347, no. 6219 (January 15, 2015): 233–34. http://dx.doi.org/10.1126/science.aaa5056.

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Mueller, K. L. "Interfering with Interferons." Science Signaling 6, no. 268 (March 26, 2013): ec75-ec75. http://dx.doi.org/10.1126/scisignal.2004169.

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Simpson, S. "Interfering with Interferon." Science's STKE 2007, no. 376 (February 28, 2007): tw81. http://dx.doi.org/10.1126/stke.3762007tw81.

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Polyak, Stephen J. "Interfering with interferon." Trends in Microbiology 7, no. 10 (October 1999): 401. http://dx.doi.org/10.1016/s0966-842x(99)01592-9.

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Dissertations / Theses on the topic "Interferoni"

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DETTORI, BEATRICE. "Effetti immunoregolatori degli interferoni di prima classe sull’attivita’ delle cellule CD4+CD25- t helper e delle cellule CD4+CD25+ Treg." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/1277.

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L’IFN-α è un mediatore di notevole importanza della risposta immunitaria. Tale citochina è in grado di indurre la risposta innata, fornendo lo stimolo per l’attivazione e la formazione della risposta immunitaria acquisita. Lo scopo principale di questo lavoro è determinare se e come IFNα è coinvolto nell’attivazione delle cellule CD4+CD25- T helper (Th) e valutare l’effetto dell’IFN-α sull’attività soppressoria delle cellule CD4+CD25+ T regolatorie (Treg) murine. I nostri risultati mostrano come IFNα promuova la produzione di IL-2 da parte delle cellule CD4+CD25- Th, quando stimolate in presenza di APC. Nonostante ciò, l’abilità di queste cellule nel rispondere allo stimolo proliferativo trasdotto da IL-2 viene inibito. IL-2 è una citochina nota per essere stimolo proliferativo per le cellule CD4+CD25+ Treg. Quando le cellule CD4+CD25+ Treg vengono co-incubate in presenza di IFNα e IL-2, la proliferazione cellulare appare inibita. Inoltre IFNα sembra ridurre l’attività soppressoria delle cellule Treg. In conclusione i nostri risultati dimostrano che IFNα agendo direttamente sulle cellule APC e riducendo l’attività delle cellule CD4+CD25+ Treg sostengono e guidano l’attivazione delle cellule CD4+CD25- Th.
Type I IFNs are central to a vast array of immunological functions. Their early induction in innate immune responses provides one of the most important priming mechanisms for the subsequent establishment of acquired immune responses. The outcome is either promotion or inhibition of these responses, but the conditions under which one or the other prevails remain to be defined. The main objective of the present study has been to determine the involvement of IFN on murine CD4+ CD25- Th cell activation, as well as to define the role played by this cytokine on CD4+ CD25+ Treg cell proliferation and function. Although IFN induces CD4+ CD25- Th cells co-incubated with APCs to produce large amounts of IL-2, at the same time their ability to respond to its proliferative effects is prevented. Moreover, in medium supplemented with IFN, IL-2 induced CD4+ CD25+ Treg cell proliferation is also inhibited. Notably, IFN also leads to a decrease of the CD4+ CD25+ Treg cell suppressive activity. Altogether, these findings indicate that trough a direct effect on APC activation and by affecting CD4+ CD25+ Treg cell- mediated suppression, IFN promotes and drives CD4+ CD25- Th cell activation.
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SPOSITO, BENEDETTA. "Type III Interferons: Running Interference with Mucosal Repair." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2023. https://hdl.handle.net/10281/402377.

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Gli interferoni (IFN) sono mediatori e regolatori fondamentali della risposta immunitaria dell'ospite a virus e ad altri agenti microbici. Gli IFN di tipo I e di tipo III (o IFN-λ) sono tra le prime citochine ad essere indotte in seguito a infezioni virali. Il legame tra gli IFN e i rispettivi recettori attiva vie di trasduzione del segnale simili tra loro che inducono l'espressione di geni stimolati dagli IFN (ISG) con funzioni antivirali. La caratteristica principale che rende ciascuna di queste famiglie di IFN unica e non ridondante è l'esistenza di recettori distinti che fanno sì che gli IFN-I attivino una risposta ubiquitaria e che gli IFN-III agiscano esclusivamente sulle cellule epiteliali e su un sottoinsieme di cellule immunitarie. Ulteriori distinzioni riguardano la natura meno infiammatoria degli IFN-III e la loro induzione solitamente anticipata rispetto a quella degli IFN-I. Pertanto gli IFN-III sono considerati i difensori di prima linea delle mucose con la capacità di attivare una risposta antivirale precoce senza causare danno tissutale. Se la loro azione risulta insufficiente a contenere l’infezione, il sistema passa all’induzione degli IFN-I, i quali generano una risposta antivirale e infiammatoria più potente e a livello sistemico, che tuttavia può portare ad immunopatologia. Nel corso della mia tesi ho verificato l'ipotesi secondo cui anche gli IFN-III possano causare immunopatologia, in particolare durante infezioni virali delle vie respiratorie e in contesti di danno all’epitelio gastrointestinale in malattie infiammatorie croniche intestinali e lesioni da radiazioni. In primo luogo, io e i miei colleghi abbiamo dimostrato che in un polmone in cui è stata indotta una risposta antivirale, gli IFN-III prodotti dalle cellule dendritiche inibiscono la proliferazione delle cellule epiteliali portando ad una compromissione del rigenerazione della barriera e ad un aumento della suscettibilità ad infezioni batteriche. In seguito abbiamo analizzato la produzione di IFN lungo il tratto respiratorio di pazienti affetti da COVID-19. Abbiamo trovato che, nelle alte vie aeree, l'espressione di IFN-I/III correla con la carica virale e che negli anziani, che presentano un maggiore rischio di sviluppare una patologia severa, questa correlazione è più debole o assente. Una forte espressione di IFN-λ1, IFN-λ3 e ISG caratterizza le alte vie aeree di pazienti con sintomatologia lieve, mentre risultano fortemente espressi gli IFN-I, IFN-λ2 e un insieme di geni antiproliferativi e proapoptotici lungo tutto il tratto respiratorio di pazienti ospedalizzati, suggerendo che possano ostacolare il processo di riparazione dell’epitelio. Infine, abbiamo dimostrato che gli IFN-III ritardano la rigenerazione dell'intestino tenue e del colon in seguito a danno da radiazioni o da colite indotta da destrano sodio solfato, poiché contribuiscono a indurre la morte cellulare delle cellule epiteliali tramite la formazione di un complesso proteico costituito da Z-DNA binding protein (ZBP1) e gasdermin C (GSDMC). I nostri risultati mettono in discussione il ruolo degli IFN-III come protettori delle mucose poiché indicano che quando non propriamente regolati possono causare immunopatologia. Queste evidenze portano alla necessità di progettare l’uso clinico degli IFN di tipo III in modo da evitare le loro funzioni dannose per i tessuti e massimizzarne gli effetti benefici.
Interferons (IFNs) are fundamental mediators and regulators of the host immune response to viruses and other microbial agents. Type I and type III IFNs (also known as IFN-λ) are some of the first cytokines to be induced upon detection of viral infections. Signaling through their specific receptors leads to the activation of a similar signaling cascade that triggers the expression of a common set of IFN-stimulated genes (ISGs) with antiviral effector functions. The main feature that makes each of these families of IFNs unique and nonredundant is the existence of distinct receptors that differentiate them in their ability to act on virtually every cell type (type I IFNs) or exclusively on epithelial cells and a subset of immune cells (type III IFNs). Despite inducing a widely overlapping set of genes, IFN-I can mount a stronger proinflammatory response compared to IFN-III. This, coupled with the earlier induction of IFN-III upon infection, has led to the classification of IFN-III as front-line defenders of mucosal surfaces with the ability to initiate an early antiviral response with minimal tissue-damaging effects. If their response is insufficient the system shifts to the more potent and broader-acting antiviral and inflammatory IFN-I response that can cause immunopathology. In the course of my thesis, I have tested the hypothesis that also IFN-III contribute to immunopathology at barrier sites such as the respiratory and gastrointestinal epithelia during viral infections and inflammatory bowel disease/radiation-induced injury respectively. First, my colleagues and I found that in a mouse model where we mimicked the induction of antiviral responses in the respiratory tract, IFN-III produced by lung dendritic cells inhibited the proliferation of lung epithelial cells leading to an impairment in barrier restoration and an increase in susceptibility to bacterial infections. Then we measured IFN responses along the respiratory tract of COVID-19 patients. We uncovered that in the upper airways expression of IFN-I/III correlated with viral load and elderly patients, that have a higher risk of developing severe COVID-19, had a dysregulation in the IFN response. A strong expression of IFN-λ1, IFN-λ3 and ISGs characterized the upper airways of mild patients. IFN-I and IFN-λ2 together with antiproliferative and proapoptotic genes were upregulated along all the respiratory tract of severe COVID-19 patients, suggesting that they might contribute to the impairment of epithelium restitution. Finally, we demonstrated that IFN-III delayed colon and small intestine repair after dextran sulfate sodium-induced colitis and radiation-induced injury by triggering cell death of epithelial cells via the formation of a novel protein complex that includes Z-DNA binding protein (ZBP1) and gasdermin C (GSDMC). Our findings challenge the role of IFN-III as protectors of mucosal barriers as they indicate that a dysregulated IFN-III response holds the potential to contribute to immunopathology. Therefore, the clinical use of type III IFNs should be designed in such a way that their tissue-damaging functions are avoided and their beneficial effects are maximized.
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Short, John A. L. "Defective interfering particles of parainfluenza virus subtype 5 and interferon induction." Thesis, University of St Andrews, 2015. http://hdl.handle.net/10023/7036.

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The innate immune response is the first line of defence against virus infection. Cells contain a diverse array of pathogen recognition receptors (PRRs) that are able to recognise multiple pathogen associated molecular patterns (PAMPS) that present themselves during virus infection. The RIG-I (Retinoic acid inducible–gene-I) and MDA5 (melanoma differentiation- associated gene 5) PRRs detect specific viral RNA ligands and subsequently induce the expression of the cytokine Interferon-β(IFN-β). IFN-βis secreted, acting on the infected cell and neighbouring uninfected cells to generate an antiviral state that is hostile to virus transcription, replication and dissemination, whilst also orchestrating adaptive immune responses. Given IFN-βs crucial cellular antiviral role, understanding its induction is of great importance to developing future antiviral drugs and vaccine strategies. Using A549 reporter cells in which GFP expression is under the control of the IFN-βpromoter, we show that there is a heterocellular response to parainfluenza virus 5 (PIV5) and infection with other negative sense RNA viruses. Only a limited number of infected cells are responsible for IFN-βinduction. Using PIV5 as a model, this thesis addresses the nature of the PAMPs that are responsible for inducing IFN-βfollowing PIV5 infection. The previous work has shown that PIV5 Defective Interfering particle (DI) rich virus preparations acted as a better inducer of IFN-βcompared to DI poor stocks. DIs are incomplete virus genomes produced during wild-type virus replication as a result of errors in the viral polymerase. To investigate this further, A549 Naïve, MDA5/RIG-I/LGP2 Knock down reporter cells were infected with PIV5 W3 at a low MOI to examine the inverse correlation of NP and GFP of DIs generated during virus replication and not from the initial infection. GFP+ve cells were cell sorted, and using QPCR it was found that cells that have the IFN-βpromoter activated contain large amounts of DIs relative to GFP-ve cells. This data supports the Randall group's findings that DIs generated during errors of wild-type replication by the viral RNA polymerase are the primary PAMPs that induce of IFN-β, as opposed to PAMPs being generated during normal wild-type virus replication.
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Jones, Meleri. "Interfering with interferon : developing a reporter system to study the interaction between hepatitus C viral proteins and the interferon signalling pathway." Thesis, Queen Mary, University of London, 2008. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1530.

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The aim of the project was to investigate the mechanism by which HCV evades therapeutic IFN treatment. This involved the development of novel testing systems and their application to patient samples. Initial experiments focused on flavivirus replicons and novel observations on effects of one of these replicons (dengue virus) on interferon signalling were made. The dengue replicon system was demonstrated to inhibit IFNa signalling by reducing the expression of STAT2, an essential component of the type I IFN signalling pathway. This phenomenom was then further examined in dengue virus infected human cells and again it was observed that the expression of STAT2 was reduced. The mechanism of STAT2 degradation was further explored and STAT2 expression was found to be restored using a proteasomal inhibitor. A second flavivirus replicon system involving BVDV was also developed as a reporter system, again with novel observations. The BVDV replicon system was shown to be sensitive to the antiviral effects of I FNa and was not shown to inhibit the IFNa signalling pathway. The BVDV replicon was tested as a reporter system using a well-known viral inhibitor of I FNa. The viral inhibitor, inhibited the antiviral action of IFNa on the BVDV reporter. Having developed and validated this system, the effects of a small number of patient derived samples were assessed and it was demonstrated that NS5a derived from a patient who failed to respond to IFNa treatment inhibited the effects of IFNa on the BVDV reporter. To increase the senstitivity of the assay the reporter cassette was then changed to a destabilised GFP for use in a FACS based assay.
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O’Gorman, Maurice R. G. "Reduced in vitro IgG secretion following in vivo injection of interferon (wellferon R) in multiple sclerosis patients." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/24876.

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An in vitro IgG secretion assay was developed to investigate the regulation of the humoral immune response in humans. Pokeweed mitogen (PWM), a plant lectin derived from Phytolacca americana stimulates human peripheral blood mononuclear cells (PBMNC) to divide and resting B-lymphocytes to differentiate into immunoglobulin secreting cells (ISC). This differentiation requires that both monocytes and T-lymphocytes be present in the culture system. The amount of IgG secreted by these differentiated B-lymphocytes in response to PWM appears to be the net result of a balance between the functional activity of the regulatory T-helper and T-suppressor cells. Alterations, qualitative or quantitative in any of these leukocyte subsets could conceivably alter the amount of IgG secreted by the B-lymphocyte subpopulation. We have employed this assay to investigate the immune status in a group of chronic progressive multiple sclerosis (MS) patients and to assess the immunoregulatory effects of interferon (Wellferon R, INF) administered in vivo to this selected group. Their mononuclear cells (MNC) were studied in this PWM induced IgG secretion assay before INF treatment and again after 7 days of daily sub-cutaneous injections (5 X 10⁶ u/day). Twenty patients received the interferon (INF) preparation and eighteen received normal saline. The study was carried out in a double blind manner and the code was broken only after individual results had been calculated.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Su, Leon L. "Mechanisms of STAT activation via the interferon-[alpha]/[beta] and B cell antigen receptor and immunomodulatory role of interferons on lymphocyte development /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9988315.

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Castilló, Justribó Joaquín. "Indicadores precoces de respuesta al tratamiento con interferón en pacientes con esclerosis múltiple." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/400286.

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Introducción: el tratamiento con interferón β sigue siendo la terapia inmunomoduladora más extendida en el tratamiento de la esclerosis múltiple remitente-recurrente si bien su eficacia es parcial. En ausencia de un biomarcador específico de respuesta, identificar precozmente a los pacientes que presentan un fallo terapéutico o una respuesta parcial es fundamental para plantear alternativas terapéuticas. Objetivo: estudiar la utilidad de la Multiple Sclerosis Functional Composite para evaluar el acumulo precoz de discapacidad, así como el valor de otras variables clínicas y de RM recogidas en el primer año de tratamiento para predecir la evolución en los 24 meses siguientes. Métodos: se diseñó un estudio prospectivo en pacientes con esclerosis múltiple remitente-recurrente que iniciaban tratamiento con interferón beta. Se realizó una valoración clínica (EDSS, MSFC, tasa de brotes) y por RM, al inicio y tras los 12 primeros meses de tratamiento. Durante los siguientes 24 meses se evaluó la presencia de actividad de la enfermedad (brotes o progresión) para definir el fallo terapéutico a largo plazo. Resultados: se incluyeron 165 pacientes, 127 en el subestudio con RM. El modelo de regresión logística demostró que sólo los parámetros de RM (presencia de más de 2 lesiones activas, OR 2.3, IC 95% 1.0-5.2) y las variables compuestas (Río Score ≥2, OR 4.8 IC 95% 1.6-1.4) eran capaces de identificar a los pacientes con riesgo de presentar una enfermedad activa tras el primer año de tratamiento con interferón. Conclusión: en pacientes con EMRR que inician tratamiento con interferón beta, la combinación de medidas de actividad clínica y por RM tras los 12 primeros meses, podría permitir identificar a aquellos que se beneficiarían de un cambio precoz de tratamiento.
Introduction: treatment with interferon β remains the most widespread immunomodulatory therapy in the treatment of relapsing-remitting multiple sclerosis, although its efficacy is partial. In the absence of a specific biomarker of response, early identification of patients with treatment failure or a partial response is critical to defining therapeutic strategies. Objective: To study the usefulness of the Multiple Sclerosis Functional Composite to evaluate the early accumulation of disability, as well as the value of other clinical and MRI variables in the first year of treatment to predict the evolution in the following 24 months. Methods: A prospective study was designed in patients with relapsing-remitting multiple sclerosis starting treatment with interferon beta. Clinical assessment (EDSS, MSFC, relapse rate) and MRI study at baseline and after 12 months of treatment were performed. During the next 24 months the presence of disease activity (relapses or progression) was evaluated to define the long term treatment failure. Results: 165 patients, 127 in the MRI substudy, were included. The logistic regression model showed that only RM parameters (presence of more than 2 active lesions, OR 2.3, 95% CI 1.0-5.2) and composite variables (Río Score ≥2, OR 4.8 95% CI 1.6-1.4) were able to identify patients at risk of developing active disease after the first year of treatment with interferon. Conclusion: In patients with RRMS starting treatment with beta interferon, the combination of measures of disease activity and the presence of new active lesions, may have a prognostic value to identify patients who benefits from early treatment change.
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Wang, Rijian. "Interferons and dermal fibrotic disorders, nitric oxide production and transforming growth factor-ß1 gene expression by normal and hypertrophic dermal fibroblasts and tissues after interferon treatment." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0008/NQ29122.pdf.

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Busche, Andreas. "Identifizierung und Charakterisierung von Modulatoren der Interferon-[gamma]-Antwort [Interferon-Gamma-Antwort]." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=96971954X.

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Migliorini, Adriana. "Role of interferon-α and interferon-β in glomerular injury and repair." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-168014.

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Obwohl die immunstimulatorischen Effekte viraler Nukleinsäursen, wie auch IFN -α und IFN-β, während Virusinfektionen eine wichtige Rolle spielen, ist wenig über ihre Funktion bei viraler Glomerulonephritis, wie beispielsweise HIV Nephropathie, bekannt. Virusinfektionen aktivieren, vor allem mittels IFN-α und IFN-β Produktion eine systemische antivirale Immunantwort. Es wurde gezeigt, dass diese inflammatorischen Zytokine einen pleiotropen immunmodulatorischen Effekt auf renale Mesangialzellen ausüben, was direkt zu glomerulären Krankheiten führt. Aber es ist bisher nicht bekannt, ob die viralen Nukleinsäuren und Typ I IFN einen Effekt auf die glomerulären Epithelzellen haben. (z.B. Podozyten und PECs). Um den Effekt von Nukleinsäuren auf Podozyten und PECs zu erforschen, stimulierten wir diese Zellen mit synthetischen dsDNA-(poly-dAdT) Komplexen mit lipofectamine, um eine virale Infektion zu imitieren. Wir haben herausgefunden, dass dsDNA stetig viele IFN-stimulierte Gene in Podozyten und PECs induziert. Desweitern haben wir herausgefunden, dass dsDNA die PECs Proliferation mindert und die CD24+/CD133+PECs Differenzierung zu ausgereiften Podozyten inhibiert. Um unsere Hypothese, dass deis aufgrund von der Sekretion von IFN-α und IFN-β passiert ist, zu bestätigen, haben wir den Effekt von diesen anitviralen Zytokinen auf PECs- und Podozyten-Homöostase etabliert. Wir haben herausgefunden, dass beide IFNs stetig Podozyten und PECs dazu anregen, stetig mehrere IFN-stimulierte Gene zu exprimieren. Trotzdem hat nur IFN-β das Podozytensterben induziert und die Permeabilität der Podozyten-Monolayer erhöht. In der Adriamycin-induzierter Nephropathie bei SCID Mäusen haben Injektionen mit IFN-α oder IFN-β die Proteinurie, den Makrophagen Influx und die Glomerulosklerose verstärkt. Trotzdem induziert nur IFN-β das mitotische Podozytensterben (katastrophale Mitose), welches zu einer reduzierten Podozytenanzahl führt. Wir haben führt, dass IFN-α einen Zellzyklusarrest in-vivo bei PECs induziert, der zur glomerulären Schädigung führt. Balb/c Mäuse, die Adriamycin gespritzt bekommen haben und täglich mit IFN-α und IFN-β behandelt wurden zeigten einen aggravierten Phänotyp mit vermehrter Proteinurie. Im Gegensatz zu dem, was an Studien in SCID Mausen gezeigt wurde, war der Effekt auf die Proteinurie nach IFN-α Behandlung prominenter bei Balb/c Mäusen, verglichen mit IFN-β. Deshalb haben Typ I IFNs einen deutlichen Effekt auf Podozyten und Parietalzellen. Zusammen fördern die Typ I IFNs die Glomerulosklerose durch verstärkten Untergang der Podozyten sowie durch Unterdrückung ihrer Regeneration aus Vorläuferzellen.
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Books on the topic "Interferoni"

1

The story of interferon: The ups and downs in the life of a scientist. Singapore: World Scientific, 1998.

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Joyce, Taylor-Papadimitriou, ed. Interferons, their impact in biology and medicine. Oxford: Oxford University Press, 1985.

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Joyce, Taylor-Papadimitriou, ed. Interferons: Their impact in biology and medicine. Oxford: Oxford University Press, 1985.

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1940-, Stewart William E., and Schellekens Huub, eds. The biology of the interferon system 1985: Proceedings of the 1985 TNO-ISIR Meeting on the Interferon System, held in Clearwater Beach, Florida, USA on 13-18 October, 1985. Amsterdam: Elsevier Science, 1986.

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E, Stewart William, Schellekens Huub, International Society for Interferon Research., and Nederlandse Centrale Organisatie voor Toegepast-Natuurwetenschappelijk Onderzoek., eds. The biology of the interferon system 1985: Proceedings of the 1985 TNO-ISIR Meeting on the Interferon System held in Clearwater Beech, Florida, USA on 13-18 October, 1985. Amsterdam: Elsevier Science, 1986.

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Holger, Kirchner, Schellekens Huub, Nederlandse Centrale Organisatie voor Toegepast-Natuurwetenschappelijk Onderzoek., and International Society for Interferon Research., eds. The biology of the interferon system 1984: Proceedings of the 1984 TNO-ISIR Meeting on the Interferon System, held in Heidelberg, Federal Republic of Germany, on 21-25 October 1984. Amsterdam: Elsevier Science, 1985.

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K, Cantell, Schellekens Huub, International Society for Interferon Research., and Nederlandse Centrale Organisatie voor Toegepast-Natuurwetenschappelijk Onderzoek., eds. The Biology of the interferon system 1986: Proceedings of the 1986 ISIR-TNO meeting on the interferon system, 7-12 September 1986, Dipoli Congress Center, Espoo, Finland. Dordrecht: Nijhoff Publishers, 1987.

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1944-, Stringfellow Dale A., ed. Clinical application of interferons and their inducers. 2nd ed. New York: Dekker, 1986.

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Razelle, Kurzrock, and Talpaz Moshe 1947-, eds. Interferons: Basic principles and clinical applications. Austin: R.G. Landes Co., 1993.

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Anthony, Meager, ed. The Interferons: Characterization and application. Weinheim: Wiley-VCH, 2006.

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Book chapters on the topic "Interferoni"

1

Kotenko, Sergei V., and Raymond P. Donnelly. "Type III Interferons: The Interferon-λ Family." In The Interferons, 141–63. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/3527608206.ch6.

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Samuel, Charles E., and Keiko Ozato. "Induction of interferons and interferon-induced genes." In Cytokine Yearbook Volume 1, 183–87. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-1616-6_5.

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Jacobsen, H. "Struktur und Wirkung von Interferonen." In Interferone, 1–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-93383-7_1.

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Otto, U., S. Conrad, H. Baisch, and G. Klöppel. "Zur Evaluierung der Interferone im Nacktmausmodell: Möglichkeiten und Ergebnisse." In Interferone, 156–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-93383-7_10.

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Pralle, H. W. "Non Hodgkin-Lymphome und Interferon-Therapie eingeschlossen Haarzell-Leukämie, ausgeschlossen Multiples Myelom." In Interferone, 167–201. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-93383-7_11.

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Ludwig, H. "Interferon in der Behandlung des multiplen Myeloms." In Interferone, 202–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-93383-7_12.

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Niederle, N. "Zur Behandlung myeloproliferativer Syndrome mit Interferonen." In Interferone, 215–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-93383-7_13.

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von Wussow, P. "Interferontherapie bei ausgewählten soliden Tumoren." In Interferone, 234–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-93383-7_14.

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Schmitz-Dräger, B. J., and R. Ackermann. "Die topische Behandlung solider Tumoren mit Interferonen." In Interferone, 269–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-93383-7_15.

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Lohmeyer, J. "AIDS und Interferone." In Interferone, 288–302. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-93383-7_16.

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Conference papers on the topic "Interferoni"

1

Lau, Eric, Giuseppina Claps, David S. Hoon, and Ze'ev A. Ronai. "Abstract 4091: Interfering with interferon: An axis of ATF2-mediated chemoresistance." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4091.

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Moneta, Gian Marco, Claudia Bracaglia, Ivan Caiello, Raffaele Pecoraro, Chiara Farroni, Fabio Basta, Luisa Bracci-Laudiero, Rita Carsetti, Fabrizio De Benedetti, and Emiliano Marasco. "AB0185 INTERFERON-Γ AMPLIFIES IMMUNE RESPONSE MEDIATED BY TYPE I INTERFERONS IN PAEDIATRIC SYSTEMIC LUPUS ERYTHEMATOSUS AND CORRELATES WITH DISEASE ACTIVITY." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7613.

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Iravantchi, Yasha, Yang Zhang, Evi Bernitsas, Mayank Goel, and Chris Harrison. "Interferi." In CHI '19: CHI Conference on Human Factors in Computing Systems. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3290605.3300506.

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"01 Targeting type I interferons." In 8th ANNUAL MEETING OF THE LUPUS ACADEMY, Warsaw, Poland, September 6–8, 2019. Lupus Foundation of America, 2019. http://dx.doi.org/10.1136/lupus-2019-la.13.

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Tsai, Yu-Chen, Sidney Pestka, Lu-Hai Wang, Loren W. Runnels, and Leroy F. Liu. "Abstract 3438: Oncogenes-induced interferon-beta: modulation of tranformation phenotypes through interferon-ISG15 autocrine signaling." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3438.

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"401 Type I interferon in NPSLE." In LUPUS 21ST CENTURY 2022 CONFERENCE, Abstracts of Sixth Scientific Meeting of North American and European Lupus Community, Tucson, AZ, USA – September 20–23, 2022. Lupus Foundation of America, 2022. http://dx.doi.org/10.1136/lupus-2022-lupus21century.13.

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Do, Hieu T., Tobias J. Oechtering, Mikael Skoglund, and Mai Vu. "Gaussian interfering relay channels." In 2013 Asilomar Conference on Signals, Systems and Computers. IEEE, 2013. http://dx.doi.org/10.1109/acssc.2013.6810649.

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Bauer, Eileen, and Philip M. Bauer. "A Novel Role For Interferon Response Factor 3 And Interferon Alpha In The Development Of Pulmonary Hypertension." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4754.

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Fitriani, Rani Siti, and Riva Nabila. "INTERFERENSI BAHASA INDONESIA SEBAGAI BAGIAN DARI RUMPUN BAHASA AUSTRONESIA." In Seminar Nasional Arkeologi 2019. Balai Arkeologi Jawa Barat, 2020. http://dx.doi.org/10.24164/prosiding.v3i1.22.

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Perubahan sosial budaya di masyarakat membawa perubahan pada perkembangan bahasa Indonesia sebagai bagian dari rumpun bahasa Austronesia. Interferensi bahasa Indonesia merupakan salah satu bentuk dari perkembangan bahasa Austronesia yang terjadi pada penutur bilingual atau multilingual dalam masyarakat heterogen. Interferensi dipengaruhi oleh tiga usur yaitu, bahasa sumber, bahasa resipien, dan importasi. Penelitian ini untuk mendeskripsikan interferensi bahasa Indonesia ditinjau dari gejala bahasa. Teori yang digunakan dalam penelitian ini adalah interferensi Weinreich (1968) dan teori tentang akar melayu Mahayana (2010). Data kebahasaan yang dijadikan sumber penelitian ini diperoleh dengan teknik pengumpulan data berupa, wawancara, simak, Metode penelitian ini menggunakan metode deskriptif. Hasil penelitian ini menunjukkan bahwa interferensi dalam bahasa Indoenesia sebagai bagian dari rumpun bahasa Austronesia terdiri dari bentukan kata seperti penghilangan fonem dan penambahan fonem.
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Skums, P., D. S. Campo, Z. Dimitrova, G. Vaughan, D. T. Lau, and Y. Khudyakov. "Modelling differential interferon resistance of HCV quasispecies." In 2011 IEEE International Conference on Bioinformatics and Biomedicine Workshops (BIBMW). IEEE, 2011. http://dx.doi.org/10.1109/bibmw.2011.6112367.

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Reports on the topic "Interferoni"

1

Havell, Edward A. Actions of Interferons on Macrophages. Fort Belvoir, VA: Defense Technical Information Center, June 1985. http://dx.doi.org/10.21236/ada157006.

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Bello, Jake, and Judith O'Malley. Interferon Inducers against Infectious Diseases. Fort Belvoir, VA: Defense Technical Information Center, April 1989. http://dx.doi.org/10.21236/adb134571.

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Bello, Jake, and Judith O'Malley. Interferon Inducers against Infectious Diseases. Fort Belvoir, VA: Defense Technical Information Center, July 1990. http://dx.doi.org/10.21236/ada231360.

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Levi, G. D. Jr, and K. E. Cheeks. Effects of interfering constituents on tritium smears. Office of Scientific and Technical Information (OSTI), December 1993. http://dx.doi.org/10.2172/10161891.

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Arlinghaus, Ralph B. Interfering Breast Cancer Metastases by Blocking NGAL Function. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada524471.

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Sastre, Adolfo G., and Connie S. Schmaljohn. Interferon Antagonism as a Common Virulence Factor of Hemorrhagic Fever Viruses. Fort Belvoir, VA: Defense Technical Information Center, February 2009. http://dx.doi.org/10.21236/ada494593.

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Johnson, Howard M. Interferon Agonists/Mimetics as Therapeutics for Smallpox and Other Respiratory Viruses. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada455389.

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Ivanova, Sonya, Raliza Skrobanska, Vera Kolyovska, Ivan Milanov, Valentina Dimitrova, and Veneta Bojinova. Neutralizing Antibodies against Interferon‑beta in Bulgarian Adolescent Multiple Sclerosis Patients. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, September 2018. http://dx.doi.org/10.7546/crabs.2018.09.15.

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Kozina, Carol L., Matthew Wallace Moorman, Catherine Branda, Meiye Wu, Ronald Paul Manginell, James Bryce Ricken, Conrad D. James, Oscar A. Negrete, Milind Misra, and Bryan D. Carson. Investigation of type-I interferon dysregulation by arenaviruses : a multidisciplinary approach. Office of Scientific and Technical Information (OSTI), September 2011. http://dx.doi.org/10.2172/1029825.

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Sastre, Adolfo G., and Connie S. Schmaljohn. Interferon Antagonism as a Common Virulence Factor of Hemorrhagic Fever Viruses. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada479293.

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